Antithrombotic therapy plays a major role in the treatment and prevention of MI and unstable angina which are collectively referred to as acute coronary syndromes (ACS). Antithrombotic therapy, if present at the time of a plaque rupture (i.e., aspirin) or administered acutely at the time of a clinical event (i.e., aspirin or heparin) can limit or partly prevent the local thrombosis from progressing to a complete occlusion (i.e., an MI). Over a period of daysor weeks, antithrombotic therapy allows endogenous fibrinolysis to dissolve the acute thrombosis, allows passivation of the lesion, and restores the acute lesion to a stable plaque. Antiplatelet agents that are more potent than aspirin are now available; these agents are antagonists to platelet glycoprotein IIb/IIIa (GP IIb/IIIa). GP IIb/IIIa is the platelet fibrinogen receptor and plays an essential role in platelet aggregation. GP IIb/IIIa antagonists complete with fibrinogen for binding to GP IIb/IIIa and thereby interfere with platelet aggregation. An oral GP IIb/IIIa antagonist, Ro 48-3657 (also known as G7333), has been developed by scientists at F. Hoffman-LaRoche Ltd. and Genentech, Inc. and provides the potential of long-term outpatient therapy. The goal of this Phase II study, called TIMI 12, is to identify dose regimens that will achieve high-grade and medium-grade inhibition of ADP- induced platelet aggregation in post ACS sbujects, and also to determine if these dose regimens are tolerable. Patient will be randomized between doses of Ro 48-3657, ASA, or placebo. Pills will be given bid for 28 days and followed up on day 7, 14 and 28. A clinic visit will take place on day 7, follow-up phone call on day 14 and rehospitalization on day 28 for blood and urine sample to determine dose response.